Description

• Phases of the hair follicle cycle
  • Anagen phase (growth phase): 90% scalp hair follicles, lasts 2 to 6 years
  • Catagen phase (transition phase): regression of follicle, <1% follicles, lasts 3 weeks
  • Telogen phase (resting phase): club hair ready for shedding, lasts 2 to 3 months
• Scarring (cicatricial) alopecia
  • Inflammatory disorders leading to permanent follicle destruction and hair loss
  • Includes lymphocytic, neutrophilic, and mixed cicatricial alopecia
• Nonscarring (noncicatricial) alopecia
  • Mild or no inflammation, no destruction of follicle
  • Includes focal (alopecia areata [AA], traction alopecia), patterned (androgenic alopecia, female pattern hair loss), or diffuse hair loss (telogen effluvium, anagen effluvium)
• Structural hair disorders: Brittle hair from abnormal hair formation/external insult

Epidemiology

Prevalence

• Androgenic alopecia:
  • In males, 30% Caucasian by 30 years of age, 50% by 50 years of age, and 80% by 70 years of age
  • In females, 70% of women >65 years of age
• AA: 1/1,000 with lifetime risk 1–2%; men and women are affected equally.
• Scarring alopecia: rare, 3–7% of all hair disorder patients

Etiology and Pathophysiology

• Scarring (cicatricial) alopecia
  • Inflammatory disorders leading to permanent destruction of the follicle
  • Slick smooth scalp without follicles evident
  • Three subtypes based on inflammation: lymphocytic, neutrophilic, and mixed
  • Primary scarring includes discoid lupus, lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, acne keloidalis nuchae, folliculitis decalvans, dissecting cellulitis of scalp, primary fibrosing, among others
  • Secondary scarring from infection, neoplasm, radiation, surgery, and other physical trauma, including tinea capitis
  • Central centrifugal cicatricial alopecia is the most common form of scarring hair loss in African American women; etiology unknown but possibly from hair care practices
• Nonscarring (noncicatricial) alopecia
  • Focal hair loss
    • AA: patchy hair loss, usually autoimmune, T cell–mediated inflammation resulting in premature transition to catagen and then telogen phases
      • May progress to alopecia totalis (entire scalp) or alopecia universalis (loss of all hair)
      • Nail disease frequently seen (10–20% of patients with AA)
      • High psychiatric comorbidity
    • Alopecia syphilitica: “moth-eaten” appearance, secondary syphilis
    • Pressure-induced alopecia: hair loss from long periods of pressure on one area of scalp
    • Temporal triangular alopecia: congenital patch of hair loss in temporal area
    • Traction alopecia: due to physical stressor of tight braids, ponytails, hair weaves
  • Patterned hair loss
    • Androgenic alopecia: hair transitions from terminal to vellus hairs
    • Male pattern hair loss: thinning in bitemporal or vertex areas (Hamilton-Norwood Scale, stages I to VII); results from increased androgen receptors, and increased 5-α reductase leads to increased testosterone conversion in follicle to dihydrotestosterone (DHT); this leads to decreased follicle size and vellus hair
    • Female pattern hair loss: thinning on frontal and vertex areas; unclear etiology, possible association with polycystic ovarian syndrome, adrenal hyperplasia, and pituitary hyperplasia
  • Trichotillomania: intentional pulling of hair from scalp; presents various patterns
• Diffuse
  • Telogen effluvium: sudden shift of many follicles from anagen to telogen phase, resulting in decreased hair density but not bald areas
    • May follow major stressors, including childbirth, injury, illness; occurs 2 to 3 months after event
    • Can be chronic with ongoing illness (SLE, renal failure, IBS, HIV, thyroid/pituitary dysfunction)
    • Adding or changing medications (oral contraceptives, anticoagulants, anticonvulsants, SSRIs, retinoids, β-blockers, ACE inhibitors, colchicine, cholesterol-lowering medications, etc.)
    • Malnutrition from malabsorption, eating disorders; poor diet can contribute.
  • Anagen effluvium
    • Interruption of the anagen phase without transition to telogen phase; days to weeks after inciting event
    • Chemotherapy is the most common trigger. Radiation, anticancer drugs, and severe protein-calorie malnutrition can also trigger.
• Inherited and acquired structural hair disorders
  • Multiple inherited hair disorders including Menkes disease, monilethrix, and so forth; these result in the formation of abnormal hairs that are weakened.
  • May also result from chemical or heat damaging from hair processing treatments

Genetics
Family history of early patterned hair loss is common in androgenic alopecia, also in AA.

Risk Factors

• Genetic predisposition
• Chronic illness including autoimmune disease, infections, cancer
• Physiologic stress including pregnancy and childbirth
• Poor nutrition
• Medication, chemotherapy, radiation
• Hair chemical treatments, braids, weaves/extensions

General Prevention

Minimize risk factors if possible.

Commonly Associated Conditions

• See “Etiology and Pathophysiology.”
• Vitiligo—4.1% patients with AA, may be the result of similar autoimmune pathways